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Effect of N-acetylcysteine on vasospasm in subarachnoid hemorrhage

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Vasospasm remains an extremely serious complication that affects patients presenting with subarachnoid hemorrhage (SAH) due to ruptured intracranial aneurysms. The current therapeutic armamentarium is still insufficient in many cases, and the search for new therapies is necessary. In this study, we evaluated the effect of N-acetylcysteine (NAC) on cerebral arterial vasospasm using an experimental model. Twenty-four wistar rats were divided into 4 groups: [1] Control, [2] SAH, [3] SAH+NAC and [4] SAH+Placebo. The experimental model employed double subarachnoid injections of autologous blood. The proposed dose of NAC was 250 mg/kg intraperitoneally per day. We analyzed the inner area of the basilar artery to assess the action of NAC. The experimental model proved to be very adequate, with a mortality rate of 4%. The inner area of the basilar artery in the SAH group showed significant difference to the control group (p=0.009). The use of NAC significantly reduced vasospasm as compared to the untreated group (p=0.048) and established no significant difference to the control group (p=0.098). There was no significant improvement with the administration of placebo (p=0.97). The model of the dual hemorrhage proved to be very useful for vasospasm simulation, with overall low mortality. The administration of NAC significantly reduced vasospasm resulting from SAH, and may represent a new therapeutic alternative.
Title: Effect of N-acetylcysteine on vasospasm in subarachnoid hemorrhage
Description:
Vasospasm remains an extremely serious complication that affects patients presenting with subarachnoid hemorrhage (SAH) due to ruptured intracranial aneurysms.
The current therapeutic armamentarium is still insufficient in many cases, and the search for new therapies is necessary.
In this study, we evaluated the effect of N-acetylcysteine (NAC) on cerebral arterial vasospasm using an experimental model.
Twenty-four wistar rats were divided into 4 groups: [1] Control, [2] SAH, [3] SAH+NAC and [4] SAH+Placebo.
The experimental model employed double subarachnoid injections of autologous blood.
The proposed dose of NAC was 250 mg/kg intraperitoneally per day.
We analyzed the inner area of the basilar artery to assess the action of NAC.
The experimental model proved to be very adequate, with a mortality rate of 4%.
The inner area of the basilar artery in the SAH group showed significant difference to the control group (p=0.
009).
The use of NAC significantly reduced vasospasm as compared to the untreated group (p=0.
048) and established no significant difference to the control group (p=0.
098).
There was no significant improvement with the administration of placebo (p=0.
97).
The model of the dual hemorrhage proved to be very useful for vasospasm simulation, with overall low mortality.
The administration of NAC significantly reduced vasospasm resulting from SAH, and may represent a new therapeutic alternative.

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